Table 1.
Studies utilizing animal and/or cell-culture models to explore the impacts of common pharmacological drugs on H2S homeostasis.
| Drug Used | Study Type | Consequence | Reference |
|---|---|---|---|
| NSAID: Indomethacin (10 mg/kg/day) and Ketoprofen (30 mg/kg/day) | Animal study: male Wistar rats | ↓ Gastric H2S generation and CSE expression/activity in the gastric mucosa of rat, leading to exacerbate mucosal damage. | [82] |
| Aspirin (10 mg during five days) | Animal study: mice | ↑ H2S in liver and brain of mice. | [83] |
| NSAID: Diclofenac (50 μmol/kg/day) | Animal study: male Wistar rats | ↓ Serum H2S and ↓ expression of CSE and CBS in the stomach of male Wistar rats | [84] |
| NSAID: Aspirin (10 mg/kg/ip) | Animal study: female albino Swiss mice | ↓ H2S levels in the liver of animals | [85] |
| NSAID: Aspirin (10–100 mg/kg); Indomethacin (10 mg/kg); Diclofenac (100 mg/kg); or Ketoprofen (30 mg/kg), | Animal study: mice | ↓ CSE expression in the GI tract enhances susceptibility of FXR−/− mice to damages caused by Aspirin and NSAIDs | [81] |
| Aspirin (200 mg/kg) | Animal study: male Sprague-Dawley rats | ↓ H2S concentration in gastric tissues but had no effect on plasma H2S concentrations | [86] |
| Aspirin (50 mg/kg/day) | Animal study: mice | ↓ Gastric expression of CBS and CSE mRNA by 60–70% leading to gastric injury. | [87] |
| Aspirin (125 mg/kg/ig) | Animal study: male Wistar rats | ↓ CSE protein expression and H2S production, and ↑ CBS protein expression, in gastric mucosal tissues, causing gastric lesions. | [88] |
| NSAID: Naproxen (20 mg/kg/day) | Animal study: Wistar rats | ↑ Gastric mucosal protein expression of CSE was observed when compared to controls, while no effect was noticed on CBS and 3-MST. | [89] |
| Aspirin (200 mg/kg/day) | Animal study: male Kunming mice | ↓ H2S production in the gastric mucosa and caused gastric mucosal injury.↓ gastric GSH levels leading to dysregulate the endogenous redox status. | [90] |
| NSAID: Ketoprofen (10 mg/kg/day) | Animal study: rats | ↓ H2S levels in the gastric and intestinal mucosa, leading to GI toxicity. | [91] |
| Paracetamol (30 mg/kg/d) or (100 mg/kg/d) | Animal study: CBA stain female mice | ↓ brain H2S concentration compared to a control group. | [92] |
| Paracetamol (150 mg/kg) | Animal study: Wistar rats | ↓ CBS and glutathione synthase enzyme expression in the liver of treated animals | [80] |
| Paracetamol (150 mg/kg/ip) | Animal study: male C57BL/6J mice | Animal study: ↓ Protein expression of both CBS and CSE In liver tissues. | [93] |
| Anticancer drug: Cisplatin (5 mg/kg/ip) | Animal study: male Wistar rats | ↑ H2S formation and CSE expression in renal tissues of animals. | [94] |
| Anticancer drug: Cisplatin (20 mg/kg/ip) | Animal study: male C57BL/6 mice | ↓ both CBS and CSE expression in the kidneys. | [95] |
| Anticancer drug: Cisplatin | In vitro: renal proximal tubular cells | ↓ Expression level of CSE and ↓ H2S production in renal cortex tissues, which may contribute to renal toxicity. | [29] |
| Lipid lowering drug: Atorvastatin (5 mg/kg/day and 20 mg/kg/day) | Animal study: female CBA-strain mice | ↓ H2S in the liver tissue (p < 0.01), but ↑ H2S levels in the kidney, brain and heart tissues of animals. | [96] |
| Lipid lowering drug: Pravastatin (40 mg/kg/day) and Atorvastatin (20 mg/kg/day) | Animal study: male Wistar rats | ↑ H2S production in the liver of animals by 51.7% and 70.7%. | [97] |
| Lipid lowering drug: Fluvastatin (5 μM) or Atorvastatin (100 μM) | In vitro: murine raw 264.7 macrophages | ↑ mRNA and protein expression levels of CSE in concentration and time dependent manners.↑ H2S production in raw 264.7 macrophages. | [98] |
| Glucocorticoid: Dexamethasone (1.5 mg/kg/day) | Animal study: male Wistar rats | ↓ the expression of CBS, CSE and H2S production in mesenteries; leading to increase blood pressure. | [79] |
| Glucocorticoid: Dexamethasone (1–1000 nmol/L) | In vitro: macrophages cells | ↓ mRNA and protein levels of CSE and H2S production in macrophages | [99] |
| Glucocorticoid: Dexamethasone(Animal study: 1 mg/kg, i.p.(In vitro: 1–10 µM) | Animal study: male Sprague-Dawley rats.In vitro: human foetal liver cells and rat neutrophils. | Animal study: ↓ H2S concentration in both plasma and tissues.In vitro: ↓expression of CSE in both human foetal liver cells and in rat neutrophils. | [28] |
| Glucocorticoid: Dexamethasone (10 μM) | In vitro: chicken myoblasts | ↓ expression of the CSE protein in myoblasts.↓mTOR and p70S6K phosphorylation.↓ protein synthesis. | [100] |
| Glucocorticoid: Dexamethasone (1 μM) | In vitro: murine calvaria-derived osteoblastic MC3T3-E1 cell line | ↓ expression of both CBS and CSE in osteoblastic. | [101] |
| Phosphodiesterase-5 inhibitors: Sildenafil (1, 3, 10, and 30 μM) | In vitro: human tissue; bladder | ↑ H2S production in concentration and time dependent manners in human bladder dome. | [102] |
| Phosphodiesterase-4 inhibitors: Rolipram (0.1 nM–10 μM) | Pig and human bladder neck | - CSE inhibitor, DL-propargylglycine (PPG, 1 mM), ↓ the Rolipram relaxation. | [103] |
| Phosphodiesterase-4 inhibitors: Rolipram: Rofumilast (0.1, 1 and 10 µM) | Pig bladder neck | ↑ H2S production in pig bladder neck samples | [104] |